Lulu Wang, Meng Guo, Li Gao, Kai Liu, Jiawei Bai and Zhiguo Liu* Pages 2977 - 2987 ( 11 )
Introduction: The dysregulation of the c-Jun NH2-terminal kinase (JNK) pathway has been increasingly reported in human malignancies. Aberrant expression of the JNK pathway has also been implicated in the progression of Esophageal Squamous Cell Carcinoma (ESCC). However, the specific role and regulatory mechanisms of JNK2 in ESCC have not been extensively investigated.
Methods: In this study, we examined JNK2 expression in patient samples and performed experiments involving the knockdown and inhibition of the JNK2 in ESCC cell lines.
Results: Higher JNK2 expression was observed in tumor tissues compared to adjacent tissues. JNK2 overexpression was associated with advanced disease stages and poor prognosis. Furthermore, knockdown or inhibition of JNK2 in ESCC cell lines resulted in a decrease in cell proliferation and migration.
Conclusion: Additionally, a significant decrease in the expression of β-catenin and vimentin, along with an increase in the expression of Axin2, was observed upon downregulation of JNK2. Our study provides insight into the role of JNK2 in ESCC and its potential regulatory mechanism, offering a potential therapeutic strategy for ESCC patients with aberrant JNK2 expression.
JNK2, WNT, Axin2, proliferation, esophageal squamous cell carcinoma, MAPKK.